Research into sudden infant death syndrome (SIDS) has led to numerous hypotheses regarding its etiology. Growing evidence suggests that a generalized arousal deficit in early postnatal development in combination with immature or dysfunctional respiratory control mechanisms may be major determinants of this syndrome. Relatively little is known about the ontogeny of sleep-wake cycles or the processes which underlie the development of arousal state control. Contemporary models of sleep-wake regulation propose two regulatory processes. One process is circadian clock-dependent and is responsible for promoting arousal. The other is homeostatic and promotes sleep as a function of prior wake duration. We hypothesize that the ontogeny of the sleep-wake cycle depends on synchronous developmental changes in both circadian clock function and sleep homeostatic mechanisms. We further postulate that SIDS could result from delayed onset of biological clock-dependent alerting mechanisms in the presence of augmented sleep drive. We propose to investigate the role of the suprachiasmatic nuclei in promoting wakefulness during development. This will be achieved by evaluating developmental changes that occur in the sleep architecture of individual rat pups (postnatal age 14-34 days) studied longitudinally in constant conditions. Similarly designed studies conducted under light-dark cycle conditions will differentiate between the appearance of endogenous sleep-wake circadian rhythms, and sleep-wake modulations due to exogenous factors. Finally, acute sleep deprivation experiments in intact and SCN-lesioned rat pups will permit evaluation of developmental changes in compensatory responses invoked by the sleep homeostatic process. Together these studies will provide comprehensive information about the developmental time-course of the principal determinants of arousal.